[SCD-FORUM] 53E RE: Some questions about Brugada Syndrome. Dr. Perez Riera to Dr. Kam
SCD Symposium
info at scd-symposium.org
Wed Oct 18 10:24:17 ART 2006
Dear Dr Ruth Kam from Singapore. Here Andrés Ricardo Pérez Riera from
Sao Paulo Brazil.
During phase 1 of AP, although brief, it is possible to observe
several categories of important ion channels for its profile
determination: Ito1, Ito2, IKATP, ICl.swell and Na+ outward movement
through the Na+/Ca2+ exchanger operating in reverse mode (Na+/Ca2+).
The Ito1 channel, ItoA, transient outward current sensitive to 4-
aminopyridine (4-AP), calcium-independent transient outward current,
initial repolarization, Ca2+ independent, voltage-operated channel,
voltage-dependent Ca2+ independent transient outward current, Itof or
Io-fast . It is a of voltage and time dependent, besides determining
the initial phase configuration of repolarization of the AP profile,
it is fundamental in its duration (APD) and in determining the
repolarization heterogeneity in the ventricular myocardium thickness.
Some evidence point that the cloned subunit Kv4.3 is similar to the
human Ito1.
The Ito current density depends on a number of factors: age group
(absent in newborn babies), sex, heart rate (more noticeable in
bradycardia), cell type studied, localization in ventricular wall
thickness, topography of myocardium and pathologic circumstances with
or without organic substrate.
In BrS, an entity without apparently structural heart disease, with
the fast Na+ current as genetic determinant of the channelopathy, the
initial outward K+ Ito1 current and the slow inward Ca2+ current in
phase 2 are essential regarding J point and ST segment level in
surface ECG, and consequently, in triggering reentry in phase 2(RF2),
and triggering bursts of PVT/IVF.
Several drugs, such as quinidine, disopyramide, flecainide, ajmaline,
procainamide, pilsicainide, etc., by modifying the functional state
of the Ito1 current, alter J point and ST segment level in right
precordial leads or from V1 to V3 in BrS.
Rarely (8% of cases), the early repolarization syndrome (ERS) may be
confused with BrS, for presenting a Brugada-like electrocardiographic
pattern. There are clinical-electrocardiographic elements that help
in making this important differentiation.
Phase 1 of AP, of initial, early or fast repolarization, coincides
with J point in surface ECG (end of QRS complex and beginning of ST
segment), being essentially dependent on fast inward Na+ current
closure and transient opening of outward K+ currents.
During the short phase 1, several channels get started:
1) Ito1, ItoA, transient outward current sensitive to 4-
aminopyridine (4-AP), calcium-independent transient outward current,
voltage-operated channel, voltage-dependent Ca2+ independent
transient outward current, Itof or Ito-fast since it has fast
activation and inactivation kinetics. Inactivation is also time-
dependent. The Kv4.3 current has been identified as the major and
main cloned subunit similar to the Ito1 current in humans(1);
2) Ito2, Itob, Ca2+-activated current, ICl.Ca, Ca2+ activated
chloride (Cl-) current, calcium-activated transient outward chloride
current, current component of the transient outward current, 4-
aminopyridine resistant transient outward current - carried by Cl-
ions, slow activation current, Ito-s or Ito-slow, 4-AP-resistant
component;
3) Variant activated by the fall in intracellular supply of ATP
when it reaches a certain critical level (IKATP); CLcAMP or time-
independent chloride Cl- current regulated by the cAMP/adenylate
cyclase pathway. Activation of the ATP-sensitive potassium current,
IKATP, is sufficient to cause ST elevation during acute ischemia;
4) Swelling-activated Cl- current (ICl(swell)): Characteristics
and functions of the cardiac swelling-activated Cl current are
considered in physiologic and pathophysiologic settings. I(Cl,swell)
is broadly distributed throughout the heart and is stimulated not
only by osmotic and hydrostatic increases in cell volume, but also by
agents that alter membrane tension and direct mechanical stretch. The
current is outwardly rectifying, reverses between the plateau and
resting potentials, and is time-independent over the physiologic
voltage range. Consequently, I(Cl,swell) shortens APD, depolarizes,
and acts to decrease cell volume. Because it is activated by stimuli
that also activate cation stretch-activated channels, I(Cl,swell)
should be considered as a potential effector of mechanoelectrical
feedback. I(Cl,swell) is activated in ischemic and non-ischemic
dilated cardiomyopathies and perhaps during ischemia and reperfusion.
The current plays a role in arrhythmogenesis, myocardial injury,
preconditioning, and apoptosis of myocytes. As a result, I(Cl,swell)
potentially is a novel therapeutic target(2);
5) The Na+ outward movement through the Na+/Ca2+ exchanger
operating in reverse mode: The sarcolemmal Na+/Ca2+ exchanger is
regulated by intracellular Ca2+ at a high affinity Ca2+ binding site
separate from the Ca2+ transport site. The Ca2+ regulatory site is
located on the large intracellular loop of the Na+/Ca2+ exchange
protein. Secondary Ca2+ regulation with the exchanger in the forward
or Ca2+ efflux mode. The Ca2+ regulation modifies transport
properties and does not only control the fraction of exchangers in an
active state.
CHARACTERISTICS OF MODALITIES OF THE CHANNELS THAT AFFECT PHASE 1 OF AP
Ito1, IA, transient outward K+ current 1, 4-aminopyridine or 4-AP-
sensitive current, the Ca2+ independent Ito1, activated during phase
1, Itof or Ito-fast This channel activity occurs in phase 1 of AP in
early or fast repolarization. Phase 1 coincides with the J point of
surface ECG Ito1 channel is voltage-operated, and therefore, it is
opened by changes in voltage in a range around the 0mV (from +30mV to
-10mV). The Ito channel is activated or inactivated, depending on
instantaneous voltage. Thus, the activation is processed in the band
between - 30mV and +10mV. The inactivation process is time-dependent,
too.
The Ito1 current is not found in newborn babies, and it only becomes
manifest after three to five months in dogs, which explains the
absence of notch in epicardial and M cells in newborn babies (age
heterogeneity).
The predominance of the Brugada phenotype in males is a result of the
presence of a more prominent Ito in males versus females(3-4).
Male predominance of the phenotype observed in SUDS does not apply to
a large European family with a missense mutation, R367H, previously
associated with SUDS suggesting that factors other than the specific
mutation determine the gender distinction(5). According to
Antzelevitch et al, the consequences of this unequal distribution of
Ito1 channels in ventricular myocardial thickness are(6)
1) Alterations of the ST segment, variously referred to as J wave,
junctional wave, late delta wave, Osborn wave, camel-hump sign, and
hump-like deflection found characteristically in severe hypothermia.
J wave is not pathognomonic of sever hypothermia and also it has also
been described in other clinical entities not associated with
hypothermia, such as acute brain injury (subarachnoid hemorrhage)
(7);, accidental cocaine overdose(8), cardiac arrest, dysfunction of
cervical sympathetic system, hypercalcemia(9) and BrS.
2) Unequal sensitivity to drugs: acetylcholine, isoproterenol, Ca2+
antagonists, Na+ channel blockers, K+ channel openers, amiodarone;
3) Greater dependence of AP duration in epicardial cells regarding
heart rate. The epicardial AP when compared with that of endocardium
shows a smaller phase 0 amplitude, a much more prominent phase 1, and
a phase 2 amplitude that is greater than that of phase 0. Epicardial
APs, unlike those of endocardium, display a "spike and dome"
morphology that becomes progressively more accentuated at slower
stimulation rates (10);
4) AP of epicardial cells more sensitive to K+: changes in T wave.
Voltage gradients created by heterogeneities of the slow-delayed
rectifier potassium current( IKs) inscribe the T wave and T-wave
polarity and width are strongly influenced by the degree of
intercellular coupling through gap-junctions. Changes in K+ modulate
the T wave through their effect on the rapid-delayed rectifier IKr.
Alterations of IKs , IKr, I and I(Na) (fast sodium current) in long-
QT syndrome (LQT1, LQT2, and LQT3, respectively) are reflected in
characteristic QT-interval and T-wave changes; LQT1 prolongs QT
without widening the T wave. Accelerated inactivation of I(Na) on the
background of large epicardial I(to) results in ST elevation (Brugada
phenotype) that reflects the degree of severity. Activation of the
ATP-sensitive potassium current, I(K(ATP)), is sufficient to cause ST
elevation during acute ischemia.;
5) Presence of supernormal phase just in the epicardium, and not in
the endocardium;
6) In the "M" cells, the Ito1 channel is found only in the
epicardium, and not in the ventricular endocardium.
A transmural voltage gradient during initial ventricular
repolarization, which results from the presence of a prominent Ito
mediated AP notch in the epicardium, but not endocardium, manifests
as a J-wave on the ECG. The J-wave is associated with the ERS, BrS
and others entities. ST-segment elevation, as seen in BrS and acute
myocardial ischemia, cannot be fully explained by using the classic
concept of an "injury current" that flows from injured to uninjured
myocardium. Rather, ST-segment elevation may be largely secondary to
a loss of the AP dome in the epicardium, but not endocardium.
The T-wave is a symbol of transmural dispersion of repolarization.
The R-on-T phenomenon (an extrasystole originating on the T-wave of a
preceding ventricular beat) is probably due to transmural propagation
of F2R early after depolarization that could potentially initiate PVT/
VF (11).
The Ito, inward rectifier IK, IKATP, IK-Ach and delayed rectifier
potassium channels ( IKS, IKr and IKur) are blocked by quinidine.
This drug of the IA class, with intermediate kinetics of uptake and
release with the Na+ current (4 to 8 seconds), moderately reduces
maximal velocity and it extends AP, and consequently, the effective
refractory period by block of the multiple outward K+ currents in
phases 1 to 3, increasing JTc and QTc intervals and fostering the
appearance of EADs; and these in turn, foster the triggered activity
that will lead to a higher tendency to TdP. It is very important
understand that quinidine and disopyramide block the Ito1 current,
but other members of the class don't, such as procainamide and
ajmaline. This subtle difference is very significant in PVT/VF
genesis in BrS. By its nonspecific potassium channel blocking action,
quinidine may also reduce arrhythmia recurrence. Additionally, it
could improve repolarization due to its vagolytic effect (M2
muscarinic receptor block) and to the exacerbation of reflex
sympathetic tone.
Oral quinidine has a role in the treatment of electrical storm (ES)
in BrS(12-13).
The Ito1 current is more visible, causing a greater notch, during
slow cardiac rates, and it plays an important role in the early phase
of AP and it influences on phase 2, plateau or dome, and
consequently, in AP duration (APD).
Ito1 current density is very reduced and consequently, it extends AP
in genetically-conditioned and salt-induced high blood pressure, in
after-constriction hypertrophy of pulmonary artery, 21 days after
acute infarction by remodeling and in heart failure (pathologic
heterogeneity) (14).
The latter leads to a significant reduction of Ito1 density and a
marked prolongation in APD. The mechanism of this reduction is
unknown. The alpha subunit of the K+ current, a homologue of the
Drosophila Shal family, is very probably an encoder of all or a part
of the native Ito current (15).
II) Ito2, ItoB, Ca2+ activated channel, ICl.Ca, Ca2+ activated
chloride (Cl-) current, Ca2+ channel activated chloride (Cl-)
current, 4-aminopyridine-resistant transient outward current carried
by Cl- ions, slow activation Ito-s or Ito-slow current. The evidence
of the Ito2 current existence is partially founded on the
pharmacological effect of several Cl- current blockers. The Ca2+-
activated Cl(-) current [I(Cl(Ca2+] contributes to the repolarization
of the cardiac AP under physiological conditions. I(Cl Ca2+) is known
to be primarily activated by Ca2+ release from the sarcoplasmic
reticulum (SR). L-type Ca2+ current represents the major trigger for
Ca2+ release in the heart. Recent evidence, however, suggests that Ca2
+ entry via reverse-mode Na+/Ca2+ exchange promoted by voltage and/or
Na+ current may also play a role (16). The Ito2 channel could be
activated by:
1) Increase in intracellular Ca2+ concentration, which in turn
releases the sarcoplasmic reticulum cation(17);
2) Acetylcholine that hyperpolarizes potential and shortens AP.
The latter is found in the sinus node, AV node and atrial muscles;
3) Arachidonic acid and its metabolites.
The Ito2 channel is blocked by disulphonic stilbenes derivatives
(SITS-DIDS) (18);
III) Variant activated by fall in ATP supply when it reaches a given
critical level (IK ATP), CLcAMP, or time-independent chloride Cl-
current regulated by the cAMP/adenylate cyclase pathway. Activation
of the ATP-sensitive potassium current, IKATP, is sufficient to cause
ST elevation during acute ischemia;
IV) Swelling-activated Cl- current or ICl-swell. Characteristics and
functions of the cardiac swelling-activated Cl current or ICl-swell
are considered in physiologic and pathophysiologic settings. ICl-
swell is broadly distributed throughout the heart and is stimulated
not only by osmotic and hydrostatic increases in cell volume, but
also by agents that alter membrane tension and direct mechanical
stretch. The current is outwardly rectifying, reverses between the
plateau and resting potentials and is time-independent over the
physiologic voltage range. Consequently, I Cl-swell shortens APD,
depolarizes, and acts to decrease cell volume. Because it is
activated by stimuli that also activate cation stretch-activated
channels, ICl-swell should be considered as a potential effector of
mechanoelectrical feedback. ICl-swell is activated in ischemic and
non-ischemic dilated cardiomyopathies and perhaps during ischemia and
reperfusion. ICl-swell plays a role in arrhythmogenesis, myocardial
injury, preconditioning, and apoptosis of myocytes. As a result, ICl-
swell potentially is a novel therapeutic target.() This channel is
inhibited by 9-anthracene carboxylic acid. Its activation causes AP
shortening;
V) Na+ outward movement through the Na+/Ca2+ exchanger operating in
reverse mode.
This mechanism exchanges 3 Na+ cations for 1 of Ca2+. The direction
of the Na+ movement depends on membrane potential and intra and
extracellular Na+ and Ca2+ concentration. The inflow mediated by this
current of Na+/Ca2+ exchange can trigger Ca2+ release in the
sarcoplasmic reticulum system.
CHARACTERISTICS AND ROLE OF THE Ito1 CURRENT IN VENTRICULAR
REPOLARIZATION
Not all of the myocardial cells have the Ito1 current and its
concentration or density depends on the area being studied.
The myocardial cells that have a high density of this channel are
characterized for presenting a prominent notch in phase 1 of AP,
showing a profile with a spike-and-dome configuration. Thus, in the
ventricular myocardium, only the fast Purkinje fibers, the M cells of
the middle myocardium, and those of the subepicardium have a
significant notch (regional heterogeneity).
There are marked differences in phases 1 to 3 in ventricular
myocardium cells AP and contractile cells when we consider thickness.
Thus, we distinguish three areas besides the Purkinje cells present
in the cardiac conduction system. This unequal distribution of the
Ito1 current in ventricular myocardial thickness is responsible for:
1) Idiopathic J wave, Junctional wave, injury potential, late
d, Osborn wave, camel-hump sign or hump-like deflection, which could
possibly be found in the J point region of surface ECG in hypothermia
(19), brain lesion(20), over come coma, hypercalcemia(21), massive
ingestion of cocaine(22), and others. When present in right
precordial leads V1-V2 or from V1 to V3 in a patient without
structural heart disease, it is known as Brugada sign. Rarely (8% of
cases) it has been reported in the athlete as a benign Early
Repolarization Syndrome (ERS) (23);
2) Unequal sensitivity to different drugs: acetylcholine,
isoproterenol, Ca2+ antagonists, Na+ current blockers, K+ current
openers and amiodarone;
3) Higher dependency of APD of epicardial cells in relation to
heart rate changes;
4) Epicardial cellular AP, more sensitive to K+, and
consequently, there are changes in the aspect of T wave polarity;
5) Presence of supernormal phase only in the epicardium and not
in the endocardium;
6) The depth of phase 1 Ito1 dependent is more marked in the
right ventricle (RV) when compared to the left one, which explains
the higher vulnerability of the RV in arrhythmias triggering in acute
ischemia conditions(24).
In atrial cells, there are Ito currents that are opened by vagal
acetylcholine release. These currents are coupled in the
acetylcholine uptake in the sarcolemma.
BrS is considered an ion channel entity or channelopathy (25).
The main affected channels in the BrS are primarily the fast Na+
current, and secondarily the initial outward K+ current, and the L-
type slow or long-lasting calcium channel ICa-L type ICa2+-L. Others
channels affected with minor importance are Ito2, IK-ATP and IKr.
The presence of a deeply notched AP or with spike-and-dome
configuration in the epicardium of the RVOT, but not in the
endocardium, is responsible for the duration of the dome or phase 2
lasting approximately a 70% less, causing a marked decrease in APD in
the epicardium in relation to the endocardium in ventricular wall
thickness of the RVOT. The phenomenon originates a ventricular
transmural gradient due to the coved type elevation( convex to the
top) of the J point and the ST segment in the right precordial leads
V1-V2 or on anteroseptal wall V1 to V3 (Brugada sign), sometimes
followed by inverted T wave(26).. The J wave is a deflection with a
dome that appears on the ECG after the QRS complex. A transmural
voltage gradient during initial ventricular repolarization, which
results from the presence of a prominent AP notch mediated by the
transient outward potassium current or initial outward K+ current in
epicardium but not endocardium, is responsible for the registration
of the J wave on the ECG.
Another variety of J point and ST segment elevation that may be
observed in BrS is a less characteristic one, that of the saddleback
type, conditioned by just a partial loss of dome, plateau or phase 2
in the RV epicardium. In it, the degree of dispersion is minimal,
with a much lower tendency to appearance of PVT/VF (27). The coved-
type J point and ST segment elevation may rarely be observed in the
inferior wall leads in absence of hypothermia, ischemia or
electrolytic disorders in patients without structural heart disease,
configuring the so-called atypical Brugada pattern or latent type
(27-28-29-30-31). Certain blockers of the fast Na+ current, such as
Class IA and IC antiarrhythmic drugs ajmaline, procainamide,
propafenone, flecainide, pilsicadine. and acetylcholine (vagal
stimulation) (32), enhance phase 1 notch in RV epicardial cells, with
a subsequent shortening in dome or phase 2 duration. This fact
results in a non-homogeneous and more heterogeneous repolarization
dispersion in the ventricular myocardial thickness, between the
subendocardium and the subepicardium, fostering the substrate for
developing reentry in phase 2, a mechanism responsible for IPVT/IVF
in BrS. When the outward current shift is marked, premature
repolarization occur in epicardial myocardium and the resulting
gradient may precipitate P2R.
Flecainide shortens the QT interval of variant 3 of congenital long
QT syndrome (LQT3), so its oral administration has been proposed to
treat this variant. Additionally, in these patients it can cause
"Brugada-like" J point and ST segment elevation(33).
Flecainide may induce ST segment elevation in LQT3 patients, raising
concerns about the safety of flecainide therapy and demonstrating the
existence of an intriguing overlap between LQT3 and BrS(34). Low-
dose, oral flecainide consistently shortened the QTc interval and
normalized the repolarization T-wave pattern in LQT3 patients with
SCN5A:DeltaKPQ mutation(35).
A class IB sodium channel blocker, mexiletine, significantly shortens
QTc, thus preventing the appearance of TdP. Strangely, the drug does
not shorten long QT in congenital LQTS, which affects the K+ current
(HERG defect of the K+ current) or variant 2 of LQTS. Mexiletine, is
most effective in abbreviating QT interval in LQT3, but effectively
reduces transmural dispersion of repolarization (TDR) and prevents
the development of Td P in all LQT1, LQT2 and LQT3 models, suggesting
its potential as an adjunctive therapy in LQT1 and LQT2(36).
The use of drugs that inhibit the Ito1 current or that stimulate Ca2+
inward movement can decrease the degree of J point and ST segment
elevation and improve repolarization in this entity . Thus, the Ito1
blocker with 4-aminopyridine (1 to 2mmol/L) or quinidine (5 micromol/
L) increase phase 2 or dome duration and normalize ST segment
elevation preventing TV/FV(37). Oral quinidine suppress the
electrical storm and prevented VF episodes in BsS patients(38). Oral
quinidine reduces phase 1 extent mediated by Ito1, normalizing ST
segment elevation in right precordial leads or from V1 to V3. IA
class drugs that block Na+ current and additionally Ito1, such as
quinidine and disopyramide, improve ECG in BrS, while those of the
same class, such as procainamide and ajmaline, which block
exclusively the Na+ current without affecting the Ito1 current,
worsen ST segment elevation and may trigger fatal tachyarrhythmias in
BrS(39). Oral quinidine induce ECG normalization in patients with BrS
(40). Publications report the employment of the drug in malignant
forms of the entity(41). Associated with adrenergic beta1-agonist and
the parasympathetic antagonist was used (42).
The presence of mild ischemia and vagotony act sinergically with the
electrophysiologic substrate of BrS, elevating ST segment and
triggering PVT/IVF bursts. This observation suggests that the Brugada
Patients are under a higher risk of SCD in coexistence with ischemia
(43).
On the contrary, isoproterenol restores phase 2 or dome in the
epicardium, reducing J point and ST segment elevation. The
vasodilator cilostazol acts through a similar mechanism: increase ICa
+2-L, and for this reason may be effective in reducing episodes of
PVT/VF(44).For this reason, isoproterenol is the drug of choice in ES
in BrS associated with general anesthesia and cardiopulmonary
"bypass" diminishing the ST elevation in right precordial leads
disappearance of the short-coupled premature beats and in removing ES
crisis of VF(45). This ominous-sounding event consists of the
incessant appearing of recurring episodes and multiple VF or VT: 20
or more per day or 4 or more per hour, eventually observed in BrS.
The ECG pattern in BrS can be intermittent and become manifest in
latent cases due to some IA class (procainamide and ajmaline) and IC
class (flecainide) antiarrhythmic agents and by night vagotony(46)
These facts support the hypothesis that J point and ST segment
elevation and the subsequent triggering of PVT/VF are dependent of a
prominent Ito current and spike-and-dome morphology in the RV
epicardium(47).
In early repolarization syndrome (ERS), a normal benign variant,
found in 1% to 2% of the population, and 13% to 48%(48) in emergency
rooms in patients with precordial pain, J point and ST segment
elevation usually presents a concavity higher >/=1mm in limb leads
and >/=2 in precordial leads, in at least two adjacent leads and with
notch or slurring of the R terminal portion of the QRS complex,
followed by T waves of enhanced voltage and concordant polarity in
the intermediate leads from V2 to V4. The most important differential
diagnosis of ERS is pericarditis, acute infarction and acute coronary
syndromes that could be treated mistakenly with fibrinolysis or
unnecessary angiography(49). In doubtful cases, besides a careful
anamnesis, the following must be conducted: echocardiogram, enzyme
and troponin I dosage(50).
There are evident differences and potent gradients in Ito1 between
the three cardiac cell types, especially between Epi and Endo cells.
These differences are among the prominent manifestations of right
ventricular electrical heterogeneity, and may form an important ionic
basis and prerequisite for some malignant arrhythmias in the right
ventricle, including those arising from BrS and other diseases(51).
ERS can be confused as well, with ventricular aneurysm. ERS is very
frequent in athletes, in whom it is observed in more than 80% of the
cases. Rarely (8%), it can present a configuration that reminds the
Brugada sign or is Brugada-like. In such cases, the following are
elements in favor of ERS (modified from Bianco.) (23).
1) Family history: negative in ERS and frequently positive for
SCD in BrS;
2) HR: tendency to bradycardia in ERS. In BrS, heart rate is
usually normal;
3) SAQRS: in ERS it tends to be vertical, and in BrSe in a 9%
of cases it presents an extreme deviation to the left;
4) PR interval: tendency to be short or normal and mildly
depressed in ERS. In BrS, it is long and in a 50% of cases (first-
degree AV block) by increase of HV;
5) QRS duration: larger in BrS (110msec +/-2msec) than in
athletes carriers of ERS (90msec+/-1msec)
6) Transition area in precordial leads: it is usually abrupt in
ERS by counterclockwise rotation in longitudinal axis. This is not
observed in BrS;
7) Degree of ST segment elevation: much larger in BrS (4.4
+/-0.7mm) than in athletes (2.3+/-0.6mm) or non-athletes (1.2
+/-0.8mm) carriers of ERS;
8) Race: it predominates in the black race in ERS. In BrS, in
the yellow race.
9) U wave: it is usually very visible in V3 due to bradycardia
in ERS. It is not frequent in BrS.
Coincidences between BrS and benign ERS:
1) Exercise can normalize ST segment elevation;
2) Isoproterenol can normalize ST segment elevation;
3) More frequent in males;
4) Predominantly observed in young adults in productive age and
under 50 years old(54).
5) Both can have ST segment elevation concave to the top,
saddleback type, and frequently persistent;
The Ito current has a decisive role in the aspect of the early
repolarization phase. Additionally, it influences on inward and
outward movement of other ions in the next phase (phase 2) and in AP
refractoriness.
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All the best
Andrés Ricardo Pérez Riera.
Chief of Electro-Vectocardiology Sector of the Discipline of
Cardiology, ABC Faculty of Medicine (FMABC), Foundation of ABC
(FUABC) - Santo André - Sao Paulo - Brazil. Rua Sebastiao Afonso 885
- Zip Code: 044417-100- Jardim Miriam S.P Brazil
--
Dr. Sergio Dubner
President of Scientific Committee
Dr. Edgardo Schapachnik
President of Steering Committee
>
> Induction of a type I Brugada pattern during febrile states has
> been well
> described.
>
> I have also observed a few cases where a Type I Brugada pattern was
> observed
> during or shortly after a strong vagal episode, such as severe
> abdominal
> pain , or a vasovagal episode, where the individual recovered quite
> quickly
> as with a vasovagal syncope, unlike a sudden cardiac arrest
> situation. The
> ECG subsequently reverted to normal or a Type II or III pattern on a
> separate occasion.
>
> What is the mechanism of these observations and what is the
> prognosis? If
> EPS is performed, how often is VT/VF inducible?
>
> I would like to hear the opinion of the experts in this field.
>
> Sincerely
>
>
> Dr Ruth Kam
> Consultant Cardiologist and Cardiac Electrophysiologist
> Ruth Kam Heart and Arrhythmia Clinic
> #08-06, Mt Elizabeth Medical Centre
> Singapore 228510
>
> --
> Dr. Sergio Dubner
> President of Scientific Committee
>
> Dr. Edgardo Schapachnik
> President of Steering Committee
>
>
>
>
> _______________________________________________
> Scd-forum mailing list
> Scd-forum at scd-symposium.org
> http://www.grupoakros.com.ar/mailman/listinfo/scd-forum
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